Pub Date : 2001-07-01DOI: 10.1080/00039890109604468
M. Martuzzi, N. D. Tanno, R. Bertollini
Abstract Declining trends in male proportion at birth observed in several Western countries might reflect widespread exposure to pollutants capable of interfering with human reproduction. In this study, the authors describe male live birth proportion trends in 23 European countries from 1950 to 1996 (total of 305 million live births). Overall, there was a significant linearly decreasing trend of 10 fewer males per 100,000 births each year, resulting in a loss of 73,462 boys during a 47-yr period. The proportion of male births during the first 3 yr of the study period was higher than in the last 3 yr in 18 countries (i.e., 78%). Decreasing trends, which varied in slope and shape, were observed in 11 countries; no significant trend was found in 8 countries, and male birth proportion increased in 4 countries. The results of this study confirmed that the proportion of male births is declining in Europe, and differences exist by region and country. Social and cultural aggregations of countries with decreasing trends suggest that sociodemographic characteristics might be more likely to explain trends than environmental exposures to chemicals. Investigators should evaluate this hypothesis to assess the usefulness of male birth proportion as a sentinel event.
{"title":"Declining Trends of Male Proportion at Birth in Europe","authors":"M. Martuzzi, N. D. Tanno, R. Bertollini","doi":"10.1080/00039890109604468","DOIUrl":"https://doi.org/10.1080/00039890109604468","url":null,"abstract":"Abstract Declining trends in male proportion at birth observed in several Western countries might reflect widespread exposure to pollutants capable of interfering with human reproduction. In this study, the authors describe male live birth proportion trends in 23 European countries from 1950 to 1996 (total of 305 million live births). Overall, there was a significant linearly decreasing trend of 10 fewer males per 100,000 births each year, resulting in a loss of 73,462 boys during a 47-yr period. The proportion of male births during the first 3 yr of the study period was higher than in the last 3 yr in 18 countries (i.e., 78%). Decreasing trends, which varied in slope and shape, were observed in 11 countries; no significant trend was found in 8 countries, and male birth proportion increased in 4 countries. The results of this study confirmed that the proportion of male births is declining in Europe, and differences exist by region and country. Social and cultural aggregations of countries with decreasing trends suggest that sociodemographic characteristics might be more likely to explain trends than environmental exposures to chemicals. Investigators should evaluate this hypothesis to assess the usefulness of male birth proportion as a sentinel event.","PeriodicalId":8276,"journal":{"name":"Archives of Environmental Health: An International Journal","volume":"12 1","pages":"358 - 364"},"PeriodicalIF":0.0,"publicationDate":"2001-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75975286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-07-01DOI: 10.1080/00039890109604470
S. Gupta, R. Gupta, AkhilendraBhushan Gupta, Asmok K. Seth, Jagdegsh K. Bassin, Alka Gupta, M. Sharma
Abstract Given that there was documented evidence of an association between diarrhea and high nitrate ingestion, the authors examined drinking water nitrate concentration and its possible correlation(s) with methemoglobin levels, cytochrome b5 reductase activity, and recurrent diarrhea. In addition, the authors studied histopathological changes in the intestines of rabbits in an animal model. Five village areas were studied, and nitrate concentrations (expressed in mg of nitrate per liter of water) of 26,45,95,220, and 459 existed in the respective villages. The study included 88 randomly selected children who were 8 yr of age or younger; they represented 10% of the total population of each of the areas. Detailed histories of recurrent diarrhea were noted, and medical examinations were conducted. Cytochrome b5 reductase activity and methemoglobin levels were estimated biochemically. Collected data were analyzed statistically with Microsoft Excel software. In addition, the authors exposed rabbits to various levels of nitrate, and histopathological changes of the stomach and intestine (small and large) were evaluated. There was a strong relationship between nitrate concentration and recurrent diarrhea; 80% of the recurrent diarrhea cases were explained by nitrate concentration alone. In the rabbit intestines, lymphocytic infiltration and hyperplasia characterized the submucosa as nitrate concentrations increased.
{"title":"Recurrent Diarrhea in Children Living in Areas with High Levels of Nitrate in Drinking Water","authors":"S. Gupta, R. Gupta, AkhilendraBhushan Gupta, Asmok K. Seth, Jagdegsh K. Bassin, Alka Gupta, M. Sharma","doi":"10.1080/00039890109604470","DOIUrl":"https://doi.org/10.1080/00039890109604470","url":null,"abstract":"Abstract Given that there was documented evidence of an association between diarrhea and high nitrate ingestion, the authors examined drinking water nitrate concentration and its possible correlation(s) with methemoglobin levels, cytochrome b5 reductase activity, and recurrent diarrhea. In addition, the authors studied histopathological changes in the intestines of rabbits in an animal model. Five village areas were studied, and nitrate concentrations (expressed in mg of nitrate per liter of water) of 26,45,95,220, and 459 existed in the respective villages. The study included 88 randomly selected children who were 8 yr of age or younger; they represented 10% of the total population of each of the areas. Detailed histories of recurrent diarrhea were noted, and medical examinations were conducted. Cytochrome b5 reductase activity and methemoglobin levels were estimated biochemically. Collected data were analyzed statistically with Microsoft Excel software. In addition, the authors exposed rabbits to various levels of nitrate, and histopathological changes of the stomach and intestine (small and large) were evaluated. There was a strong relationship between nitrate concentration and recurrent diarrhea; 80% of the recurrent diarrhea cases were explained by nitrate concentration alone. In the rabbit intestines, lymphocytic infiltration and hyperplasia characterized the submucosa as nitrate concentrations increased.","PeriodicalId":8276,"journal":{"name":"Archives of Environmental Health: An International Journal","volume":"1 1","pages":"369 - 373"},"PeriodicalIF":0.0,"publicationDate":"2001-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76196186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-07-01DOI: 10.1080/00039890109604460
J. D. Thrasher, K. Kilburn
Abstract C-14 formaldehyde crosses the placenta and enters fetal tissues. The incorporated radioactivity is higher in fetal organs (i.e., brain and liver) than in maternal tissues. The incorporation mechanism has not been studied fully, but formaldehyde enters the single-carbon cycle and is incorporated as a methyl group into nucleic acids and proteins. Also, formaldehyde reacts chemically with organic compounds (e.g., deoxyribonucleic acid, nucleosides, nucleotides, proteins, amino acids) by addition and condensation reactions, thus forming adducts and deoxyribonucleic acid-protein crosslinks. The following questions must be addressed: What adducts (e.g., N-methyl amino acids) are formed in the blood following formaldehyde inhalation? What role do N-methyl-amino adducts play in alkylation of nuclear and mitochondrial deoxyribonucleic acid, as well as mitochondrial peroxidation? The fact that the free formaldehyde pool in blood is not affected following exposure to the chemical does not mean that formaldehyde is not involved in altering cell and deoxyribonucleic acid characteristics beyond the nasal cavity. The teratogenic effect of formaldehyde in the English literature has been sought, beginning on the 6th day of pregnancy (i.e., rodents) (Saillenfait AM, et al. Food Chem Toxicol 1989, pp 545–48; Martin WJ. Reprod Toxicol 1990, pp 237–39; Ulsamer AC, et al. Hazard Assessment of Chemicals; Academic Press, 1984, pp 337–400; and U.S. Department of Health and Human Services. Toxicological Profile of Formaldehyde; ATSDR, 1999 [references 1–4, respectively, herein]). The exposure regimen is critical and may account for the differences in outcomes. Pregnant rats were exposed (a) prior to mating, (b) during mating, (c) or during the entire gestation period. These regimens (a) increased embryo mortality; (b) increased fetal anomalies (i.e., cryptochordism and aberrant ossification centers); (c) decreased concentrations of ascorbic acid; and (d) caused abnormalities in enzymes of mitochondria, lysosomes, and the endoplasmic reticulum. The alterations in enzymatic activity persisted 4 mo following birth. In addition, formaldehyde caused metabolic acidosis, which was augmented by iron deficiency. Furthermore, newborns exposed to formaldehyde in utero had abnormal performances in open-field tests. Disparities in teratogenic effects of toxic chemicals are not unusual. For example, chlorpyrifos has not produced teratogenic effects in rats when mothers are exposed on days 6–15 (Katakura Y, et al. Br J Ind Med 1993, pp 176–82 [reference 5 herein]) of gestation (Breslin WJ, et al. Fund Appl Toxicol 1996, pp 119–30; and Hartley TR, et al. Toxicol Sci 2000, pp 100–08 [references 6 and 7, respectively, herein]). However, either changing the endpoints for measurement or exposing neonates during periods of neurogenesis (days 1–14 following birth) and during subsequent developmental periods produced adverse effects. These effects included neuroapoptosis, decreased deo
C-14甲醛通过胎盘进入胎儿组织。胎儿器官(即大脑和肝脏)中的放射性掺入比母体组织中的放射性要高。甲醛的掺入机理尚未得到充分的研究，但甲醛进入单碳循环，以甲基的形式掺入核酸和蛋白质中。此外，甲醛通过加成和缩合反应与有机化合物(如脱氧核糖核酸、核苷、核苷酸、蛋白质、氨基酸)发生化学反应，从而形成加合物和脱氧核糖核酸-蛋白质交联。必须解决以下问题:吸入甲醛后血液中会形成什么加合物(如n -甲基氨基酸)?n -甲基氨基加合物在细胞核和线粒体脱氧核糖核酸的烷基化以及线粒体过氧化反应中起什么作用?暴露于这种化学物质后，血液中的游离甲醛池不受影响，这一事实并不意味着甲醛不参与改变鼻腔以外的细胞和脱氧核糖核酸特征。在英国文献中，甲醛的致畸作用已被寻求，从怀孕第6天开始(即啮齿动物)(Saillenfait AM, et al.)。食品化学毒理学1989,pp 545-48;马丁WJ。生殖毒物，1990,pp 237-39;Ulsamer AC等。化学品危害评估;学术出版社，1984年，337-400页;以及美国卫生与公众服务部甲醛的毒理学概况;ATSDR, 1999[分别参考文献1-4])。暴露方案至关重要，可能是导致结果差异的原因。妊娠大鼠分别在(a)交配前、(b)交配中、(c)或整个妊娠期暴露。这些方案(a)增加胚胎死亡率;(b)胎儿异常增加(即隐索畸形和异常骨化中心);(c)抗坏血酸浓度降低;(d)引起线粒体、溶酶体和内质网酶的异常。酶活性的改变在出生后4个月仍然存在。此外，甲醛引起代谢性酸中毒，并因缺铁而加重。此外，在子宫内暴露于甲醛的新生儿在露天测试中表现异常。有毒化学物质致畸作用的差异并不罕见。例如，当母鼠在第6-15天接触毒死蜱时，毒死蜱不会对大鼠产生致畸作用(Katakura Y等)。Br J Ind Med, 1993, pp 176-82[文献5])妊娠(Breslin WJ, et。基金苹果毒理学1996,pp 119-30;Hartley TR等。毒物科学2000，第100-08页[分别参考文献6和7])。然而，无论是改变测量终点，还是在新生儿神经发生期间(出生后1-14天)和随后的发育期间暴露，都会产生不良影响。这些影响包括神经细胞凋亡、脱氧核糖核酸和核糖核酸合成减少、腺苷酸环化酶级联异常以及神经行为影响(Johnson DE等)。Brain Res, 1998, pp 143-47;Lassiter TL，等。毒物科学1999,pp 92-100;Chakraborti TK等。生物化学学报1993,pp 219-24;惠特尼·KD，等。苹果制药1995,pp 53-62;Chanda SM，等。药物生物化学行为1996,pp 771-76;Dam K，等。Devel Brain Res 1998, pp 39-45;坎贝尔等人。Brain Res Bull 1997, pp 179-89;熊鑫，等。毒理学杂志，苹果制药，第158-74页[参考文献8-15])。此外，沙利度胺引起的早产是一个生动的人类例子，其中动物模型和暴露时间是关键因素(Parman T等)。国家医学1999,582-85页;Brenner CA等。Mol Human Repro 1998, pp 887-92[分别参考文献16和17])。因此，在测量环境因素对胚胎、胎儿和新生儿的毒性作用时，更敏感的终点(如酶活性、活性氧的产生、暴露时间)似乎比总的terata观察结果更连贯。围产期从人体器官发生结束到新生儿期结束，大约为妊娠第28天至产后4周。因此，研究人员必须研究相似的发育阶段(例如，人类的神经发生在妊娠晚期，大鼠和小鼠的新生期发生在第1-14天，而豚鼠的行为更像人类)。最后，筛查致畸事件还应包括雌性在交配前或交配后不久的暴露。这种方案是卓有成效的，因为环境因素会对卵巢元素(例如，鞘细胞和卵子[核脱氧核糖核酸和线粒体脱氧核糖核酸])以及着床前的受精卵和胚胎产生不利影响。 线粒体脱氧核糖核酸突变和缺失发生在人类卵母细胞和胚胎(Parman T, et al.)。国家医学1999,582-85页;Brenner CA等。Mol Human Repro 1998, pp 887-92[分别参考文献16和17])。因此，外源药物很可能直接影响卵子或受精卵/胚胎或两者中的n-脱氧核糖核酸和/或线粒体脱氧核糖核酸(Thrasher JD)。Arch Environ Health, 2000年，第292-94页[此处参考文献18])，它们可以解释包括自闭症在内的各种线粒体疾病越来越多的出现(Lomard L. Med hypothesis, 1998年，第497-99页;华莱士EC。国家科学进展1994,pp 8730-46;和Giles RE等。《国家科学学报》1980,pp 6715-19[参考文献19-21])。在甲醛污染的家庭中报告了两例人类出生缺陷(Woodbury MA等)。甲醛毒性1983;第203-11页[参考文献22])。一个病例是无脑在2.76 ppm，而另一个缺陷在0.54 ppm没有表征。建议进一步观察人类出生缺陷。
{"title":"Embryo Toxicity and Teratogenicity of Formaldehyde","authors":"J. D. Thrasher, K. Kilburn","doi":"10.1080/00039890109604460","DOIUrl":"https://doi.org/10.1080/00039890109604460","url":null,"abstract":"Abstract C-14 formaldehyde crosses the placenta and enters fetal tissues. The incorporated radioactivity is higher in fetal organs (i.e., brain and liver) than in maternal tissues. The incorporation mechanism has not been studied fully, but formaldehyde enters the single-carbon cycle and is incorporated as a methyl group into nucleic acids and proteins. Also, formaldehyde reacts chemically with organic compounds (e.g., deoxyribonucleic acid, nucleosides, nucleotides, proteins, amino acids) by addition and condensation reactions, thus forming adducts and deoxyribonucleic acid-protein crosslinks. The following questions must be addressed: What adducts (e.g., N-methyl amino acids) are formed in the blood following formaldehyde inhalation? What role do N-methyl-amino adducts play in alkylation of nuclear and mitochondrial deoxyribonucleic acid, as well as mitochondrial peroxidation? The fact that the free formaldehyde pool in blood is not affected following exposure to the chemical does not mean that formaldehyde is not involved in altering cell and deoxyribonucleic acid characteristics beyond the nasal cavity. The teratogenic effect of formaldehyde in the English literature has been sought, beginning on the 6th day of pregnancy (i.e., rodents) (Saillenfait AM, et al. Food Chem Toxicol 1989, pp 545–48; Martin WJ. Reprod Toxicol 1990, pp 237–39; Ulsamer AC, et al. Hazard Assessment of Chemicals; Academic Press, 1984, pp 337–400; and U.S. Department of Health and Human Services. Toxicological Profile of Formaldehyde; ATSDR, 1999 [references 1–4, respectively, herein]). The exposure regimen is critical and may account for the differences in outcomes. Pregnant rats were exposed (a) prior to mating, (b) during mating, (c) or during the entire gestation period. These regimens (a) increased embryo mortality; (b) increased fetal anomalies (i.e., cryptochordism and aberrant ossification centers); (c) decreased concentrations of ascorbic acid; and (d) caused abnormalities in enzymes of mitochondria, lysosomes, and the endoplasmic reticulum. The alterations in enzymatic activity persisted 4 mo following birth. In addition, formaldehyde caused metabolic acidosis, which was augmented by iron deficiency. Furthermore, newborns exposed to formaldehyde in utero had abnormal performances in open-field tests. Disparities in teratogenic effects of toxic chemicals are not unusual. For example, chlorpyrifos has not produced teratogenic effects in rats when mothers are exposed on days 6–15 (Katakura Y, et al. Br J Ind Med 1993, pp 176–82 [reference 5 herein]) of gestation (Breslin WJ, et al. Fund Appl Toxicol 1996, pp 119–30; and Hartley TR, et al. Toxicol Sci 2000, pp 100–08 [references 6 and 7, respectively, herein]). However, either changing the endpoints for measurement or exposing neonates during periods of neurogenesis (days 1–14 following birth) and during subsequent developmental periods produced adverse effects. These effects included neuroapoptosis, decreased deo","PeriodicalId":8276,"journal":{"name":"Archives of Environmental Health: An International Journal","volume":"14 1","pages":"300 - 311"},"PeriodicalIF":0.0,"publicationDate":"2001-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83065818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-07-01DOI: 10.1080/00039890109604467
É. Dewailly, P. Ayotte, S. Bruneau, G. Lebel, P. Levallois, J. Weber
Abstract The authors conducted a survey during 1992 to evaluate blood levels of lead and mercury in Inuit adults of Nunavik (Arctic Québec, Canada). Blood samples obtained from 492 participants (209 males and 283 females; mean age = 35 yr) were analyzed for lead and total mercury; mean (geometric) concentrations were 0.42 μmol/l (range = 0.04–2.28 μmol/l) and 79.6 nmol/l (range = 4–560 nmol/l), respectively. Concentrations of omega-3 fatty acid in plasma phospholipids–a biomarker of marine food consumption–were correlated with mercury (r = .56, p < .001) and, to a lesser extent, with blood lead levels (r = .31, p < .001). Analyses of variance further revealed that smoking, age, and consumption of waterfowl were associated with lead concentrations (r 2 = .30, p < .001), whereas age and consumption of seal and beluga whale were related to total mercury levels (r 2 = .30, p < .001). A significant proportion of reproductive-age women had lead and mercury concentrations that exceeded those that have been reportedly associated with subtle neurodevelopmental deficits in other populations.
作者在1992年进行了一项调查，以评估Nunavik (Arctic qu忧郁，加拿大)因纽特成年人的血铅和汞水平。从492名参与者(209名男性和283名女性)获得血液样本;平均年龄= 35岁)进行铅和总汞分析;平均(几何)浓度分别为0.42 μmol/l(范围为0.04 ~ 2.28 μmol/l)和79.6 nmol/l(范围为4 ~ 560 nmol/l)。血浆磷脂中omega-3脂肪酸的浓度(海洋食物消耗的生物标志物)与汞相关(r = 0.56, p < 0.001)，在较小程度上与血铅水平相关(r = 0.31, p < 0.001)。方差分析进一步表明，吸烟、年龄和水禽的摄入量与铅浓度相关(r2 = 0.30, p < 0.001)，而年龄和海豹和白鲸的摄入量与总汞水平相关(r2 = 0.30, p < 0.001)。相当大比例的育龄妇女体内的铅和汞浓度超过了据报道在其他人群中与微妙的神经发育缺陷有关的浓度。
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Pub Date : 2001-07-01DOI: 10.1080/00039890109604456
K. Kilburn
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Pub Date : 2001-07-01DOI: 10.1080/00039890109604462
T. Aldrich, K. W. Andrews, A. Liboff
Abstract Cancer cluster studies in North Carolina identified several communities in which there existed an elevated risk of brain cancer. These findings prompted a series of case-control studies. The current article, which originated from the results of the 3rd of such studies, is focused on inclusion of the earth's own geomagnetic fields that interact with electromagnetic fields generated from distribution power lines. This article also contains an assessment of the contribution of confounding by residential (e.g., urban, rural) and case characteristics (e.g., age, race, gender). Newly diagnosed brain cancer cases were identified for a 4-county region of central North Carolina, which the authors chose on the basis of the results of earlier observations. A 3:1 matched series of cancer cases from the same hospitals in which the cases were diagnosed served as the comparison group. Extensive geographic information was collected and was based on an exact place of residence at the time of cancer diagnosis, thus providing several strategic geophysical elements for assessment. The model for this assessment was based on the effects of these two sources of electromagnetic fields for an ion cyclotron resonance mechanism of disease risk. The authors used logistic regression models that contained the predicted value for the parallel component of the earth's magnetic field; these models were somewhat erratic, and the elements were not merged productively into a single statistical model. Interpretation of these values was difficult; therefore, the modeled values for the model elements, at progressive distances from the nearest power-line segments, are provided. The results of this study demonstrate the merits of using large, population-based databases, as well as using rigorous Geographic Information System techniques, for the assessment of ecologic environmental risks. The results also suggest promise for exposure classification that is compatible with the theoretical biological mechanisms posited for electromagnetic fields.
{"title":"Brain Cancer Risk and Electromagnetic Fields (EMFs): Assessing the Geomagnetic Component","authors":"T. Aldrich, K. W. Andrews, A. Liboff","doi":"10.1080/00039890109604462","DOIUrl":"https://doi.org/10.1080/00039890109604462","url":null,"abstract":"Abstract Cancer cluster studies in North Carolina identified several communities in which there existed an elevated risk of brain cancer. These findings prompted a series of case-control studies. The current article, which originated from the results of the 3rd of such studies, is focused on inclusion of the earth's own geomagnetic fields that interact with electromagnetic fields generated from distribution power lines. This article also contains an assessment of the contribution of confounding by residential (e.g., urban, rural) and case characteristics (e.g., age, race, gender). Newly diagnosed brain cancer cases were identified for a 4-county region of central North Carolina, which the authors chose on the basis of the results of earlier observations. A 3:1 matched series of cancer cases from the same hospitals in which the cases were diagnosed served as the comparison group. Extensive geographic information was collected and was based on an exact place of residence at the time of cancer diagnosis, thus providing several strategic geophysical elements for assessment. The model for this assessment was based on the effects of these two sources of electromagnetic fields for an ion cyclotron resonance mechanism of disease risk. The authors used logistic regression models that contained the predicted value for the parallel component of the earth's magnetic field; these models were somewhat erratic, and the elements were not merged productively into a single statistical model. Interpretation of these values was difficult; therefore, the modeled values for the model elements, at progressive distances from the nearest power-line segments, are provided. The results of this study demonstrate the merits of using large, population-based databases, as well as using rigorous Geographic Information System techniques, for the assessment of ecologic environmental risks. The results also suggest promise for exposure classification that is compatible with the theoretical biological mechanisms posited for electromagnetic fields.","PeriodicalId":8276,"journal":{"name":"Archives of Environmental Health: An International Journal","volume":"11 1","pages":"314 - 319"},"PeriodicalIF":0.0,"publicationDate":"2001-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84916897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-07-01DOI: 10.1080/00039890109604457
M. Mehlman
{"title":"In Memoriam Professor Cesare Maltoni, Born: November 17, 1930 Died: January 22, 2001","authors":"M. Mehlman","doi":"10.1080/00039890109604457","DOIUrl":"https://doi.org/10.1080/00039890109604457","url":null,"abstract":"","PeriodicalId":8276,"journal":{"name":"Archives of Environmental Health: An International Journal","volume":"1 1","pages":"294 - 295"},"PeriodicalIF":0.0,"publicationDate":"2001-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87752236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-07-01DOI: 10.1080/00039890109604466
M. Benedetti, Ivano Lavarone, P. Comba
Abstract In this study, the authors sought to review available epidemiologic studies of cancer risk and its association with residence in a neighborhood characterized by industrial sites and to discuss options for future study design. The authors attempted to identify all case-control studies published from January 1980 through July 1997 in which investigators examined exposure resulting from residential proximity to an industrial site neighborhood relative to an increased risk of lung, urinary tract, and lymphohematopoietic malignancies. During these years, some authors reported significant associations between lung cancer risk and residential proximity to (a) smelters, (b) complex industrial areas, and (c) other localized emission sources. There was some evidence that leukemia and lymphomas occurred in the neighborhoods that contained industrial sites.
{"title":"Cancer Risk Associated with Residential Proximity to Industrial Sites: A Review","authors":"M. Benedetti, Ivano Lavarone, P. Comba","doi":"10.1080/00039890109604466","DOIUrl":"https://doi.org/10.1080/00039890109604466","url":null,"abstract":"Abstract In this study, the authors sought to review available epidemiologic studies of cancer risk and its association with residence in a neighborhood characterized by industrial sites and to discuss options for future study design. The authors attempted to identify all case-control studies published from January 1980 through July 1997 in which investigators examined exposure resulting from residential proximity to an industrial site neighborhood relative to an increased risk of lung, urinary tract, and lymphohematopoietic malignancies. During these years, some authors reported significant associations between lung cancer risk and residential proximity to (a) smelters, (b) complex industrial areas, and (c) other localized emission sources. There was some evidence that leukemia and lymphomas occurred in the neighborhoods that contained industrial sites.","PeriodicalId":8276,"journal":{"name":"Archives of Environmental Health: An International Journal","volume":"59 1","pages":"342 - 349"},"PeriodicalIF":0.0,"publicationDate":"2001-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84900383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-07-01DOI: 10.1080/00039890109604471
K. Hoffmann, C. Krause, B. Seifert
Abstract As part of the representative Environmental Survey in Germany in 1990–1992, investigators determined cadmium levels in blood provided by 3,965 subjects aged 25–69 yr. The investigators considered approximately 150 variables (i.e., demographics, household and occupational characteristics, environmental exposures, smoking habits, frequency of food consumption, and additional life-style features) as potential predictors in multivariate regression analysis. On the basis of the results of multivariate regression analysis, the authors derived 2 slightly different models for the prediction of blood cadmium levels in populations from West and East Germany. Both models included 3 primary predictors of blood cadmium levels. The 2 models explained 51.3% and 61.2% of the observed variance in blood cadmium levels in West and East Germany, respectively. The most important predictor was a specific indicator for smoking habits, which was determined from a separate mathematical model. In this model, the effect of smoking was considered, and the model accounted for the biological half-life of cadmium in blood.
{"title":"The German Environmental Survey 1990/92 (GerES II): Primary Predictors of Blood Cadmium Levels in Adults","authors":"K. Hoffmann, C. Krause, B. Seifert","doi":"10.1080/00039890109604471","DOIUrl":"https://doi.org/10.1080/00039890109604471","url":null,"abstract":"Abstract As part of the representative Environmental Survey in Germany in 1990–1992, investigators determined cadmium levels in blood provided by 3,965 subjects aged 25–69 yr. The investigators considered approximately 150 variables (i.e., demographics, household and occupational characteristics, environmental exposures, smoking habits, frequency of food consumption, and additional life-style features) as potential predictors in multivariate regression analysis. On the basis of the results of multivariate regression analysis, the authors derived 2 slightly different models for the prediction of blood cadmium levels in populations from West and East Germany. Both models included 3 primary predictors of blood cadmium levels. The 2 models explained 51.3% and 61.2% of the observed variance in blood cadmium levels in West and East Germany, respectively. The most important predictor was a specific indicator for smoking habits, which was determined from a separate mathematical model. In this model, the effect of smoking was considered, and the model accounted for the biological half-life of cadmium in blood.","PeriodicalId":8276,"journal":{"name":"Archives of Environmental Health: An International Journal","volume":"21 1","pages":"374 - 379"},"PeriodicalIF":0.0,"publicationDate":"2001-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86296537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-07-01DOI: 10.1080/00039890109604458
E. Richter, T. Berman
Using particulate matter with diameters of 10 mcm or less (PM10) as markers of exposure Kunzli et al. reported that annual mortality from air pollution exceeds mortality from road injury in Austria France and Switzerland. However they did not examine the role of increased speed limits and travel speeds relative to the increase in the death toll from air pollution emissions and their general effects on health. It is noted that rate of emissions of certain air pollutants [carbon monoxide (CO) oxides of nitrogen] per distance traveled increases exponentially with increases in travel speeds in private vehicles that run on petrol and in trucks and private vehicles that run on diesel fuel (PM10). In addition emissions of carbon dioxide (CO2) the major greenhouse gas increase arithmetically with increases in speed above 80 km/hour. For CO2 CO and hydrocarbons emitted by private vehicles and diesel trucks there is an approximate U- shaped relationship between speed and fuel efficiency which approaches maximum in the range of 40-75 km/hour. Therefore speed regulation of private vehicles and commercial trucking is the sine qua non for a model shift to high-speed mass transit of both persons and goods.
{"title":"Speed, Air Pollution, and Health: A Neglected Issue","authors":"E. Richter, T. Berman","doi":"10.1080/00039890109604458","DOIUrl":"https://doi.org/10.1080/00039890109604458","url":null,"abstract":"Using particulate matter with diameters of 10 mcm or less (PM10) as markers of exposure Kunzli et al. reported that annual mortality from air pollution exceeds mortality from road injury in Austria France and Switzerland. However they did not examine the role of increased speed limits and travel speeds relative to the increase in the death toll from air pollution emissions and their general effects on health. It is noted that rate of emissions of certain air pollutants [carbon monoxide (CO) oxides of nitrogen] per distance traveled increases exponentially with increases in travel speeds in private vehicles that run on petrol and in trucks and private vehicles that run on diesel fuel (PM10). In addition emissions of carbon dioxide (CO2) the major greenhouse gas increase arithmetically with increases in speed above 80 km/hour. For CO2 CO and hydrocarbons emitted by private vehicles and diesel trucks there is an approximate U- shaped relationship between speed and fuel efficiency which approaches maximum in the range of 40-75 km/hour. Therefore speed regulation of private vehicles and commercial trucking is the sine qua non for a model shift to high-speed mass transit of both persons and goods.","PeriodicalId":8276,"journal":{"name":"Archives of Environmental Health: An International Journal","volume":"12 1","pages":"296 - 297"},"PeriodicalIF":0.0,"publicationDate":"2001-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75267099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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